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C M Poser

Publications and source records attributed to C M Poser.

At least 37 records · Page 2Linked to original sources
PubMed1995

Viking voyages: the origin of multiple sclerosis? An essay in medical history.

Multiple sclerosis is most frequently found in Scandinavia, Iceland, the British Isles and the countries settled by their inhabitants and their descendants, i.e. the United States, Canada, Australia and New Zealand. This suggests that the Vikings may have been instrumental in disseminating genetic susceptibility to the disease in those areas, as well as in other parts of the world. The Vikings raided most European countries and settled in Normandy and in Sicily and southern Italy. They engaged in trade with the Arabs along the river routes to the Caucasus, to the Black and Caspian Seas, and penetrated Persia, India and probably China. They also migrated to the East and established the Russian state. Under the name Varangians, they became part of the Byzantine army and were active in all the military activities of the Byzantine Empire. They participated in the Crusades. Russians, many of Scandinavian origin also constituted a regiment of the Mongol army and roamed throughout that Empire as well. The custom of capturing and keeping or selling women and children, which was widespread in the early Middle Ages, as well as the flourishing slave trade in men, were important factors in this genetic dissemination.

Asia↗
PubMed1995

Multiphasic disseminated encephalomyelitis presenting as alternating hemiplegia.

Two cases of alternating hemiparesis are reported, one in a black Sudanese woman, the other in a Saudi man, who had two episodes of alternating hemiparesis separated in time by six and three years respectively. Based on the typical appearance of the MRI and the results of brain biopsy, the diagnosis of multiphasic disseminated encephalomyelitis was made rather than that of multiple sclerosis. This entity is also differentiated from recurrent disseminated encephalomyelitis, where the relapses are symptomatically stereotyped although the appearance of the MRI is similar and in which new lesions do not occur. Because of the unusual appearance of these MRI lesions, brain biopsy is often performed but recognising their relevance should obviate that need.

Adult↗
PubMed1995

Brain lesions in patients with multiple sclerosis: detection with echo-planar imaging.

PURPOSE: To evaluate the detection of brain lesions with echo-planar imaging relative to conventional spin-echo (SE) imaging. MATERIALS AND METHODS: In 17 patients (three men, 14 women; mean age, 31 years) with multiple sclerosis, the following were compared: single-shot proton-density- and T2-weighted and thin-section T2-weighted echo-planar, proton-density- and T2-weighted multishot echo-planar, and conventional SE sequences. Quantitative and qualitative criteria as well as lesion detectability were evaluated. The proton-density-weighted SE sequence was used as the standard of reference. RESULTS: Multishot sequences were superior to single-shot sequences in image quality and lesion detectability. With the multishot proton-density-weighted sequence, 53 of 54 large lesions and 23 of 30 small lesions were detected; with the single-shot proton-density-weighted sequence, 38 of 54 large lesions and five of 30 small lesions were detected. CONCLUSION: With multishot echo-planar sequences, detectability of large lesions is similar to that with conventional SE imaging. Susceptibility artifact is diminished in comparison to single-shot echo-planar sequences.

Adult↗
PubMed1995

Notes on the epidemiology of multiple sclerosis.

The single most important feature that determines the reliability of epidemiologic studies of multiple sclerosis (MS) is the use of well-defined, generally recognized diagnostic criteria. The long-accepted direct relationship between prevalence rates (PR) and latitude is no longer valid and has been replaced by the realization that genetic factors play an important role in the acquisition of the disease. The nature of environmental factors, which may be of more importance in influencing the clinical manifestations of the disease, remains obscure. Most potential risk factors that have been studied lack biologic plausibility. Biostatistical interpretation of epidemiologic data can only indicate possible causal relationships but cannot conclusively rule out their existence. Differences in PR among different ethnic groups in similar locations suggest that, in addition to genetic factors, there may be enhancing and/or protective influences which are probably environmental in nature. Migration studies have been interpreted as suggesting that MS is acquired before puberty and that age at migration is important in determining the risk of having clinical disease. Epidemics by age of onset vanish when recalculated on the basis of age of acquisition, and probably mean that more early and mild cases are being diagnosed. A new definition of PR is proposed, ie, onset-adjusted PR, which includes patients who had symptoms at the time of the survey, but had not yet been diagnosed as MS. However, individuals who had symptoms at the time of migration to a study area must not be included in PR.(ABSTRACT TRUNCATED AT 250 WORDS)

Emigration and Immigration↗
PubMed1994

The epidemiology of multiple sclerosis: a general overview.

Epidemiological studies of multiple sclerosis (MS) have shown the importance of genetic susceptibility factors that are modified by as yet unknown environmental influences. The often-cited interrelation between prevalence and latitude is no longer viable, with the important but unexplained exception of Australia and New Zealand. The standardization and increasing use of uniform diagnostic criteria lend new credibility to the results of MS surveys. More precise criteria are offered for symptoms of disease onset, Devic's syndrome, and progressive disease. The role of magnetic resonance imaging in the diagnosis of MS, and the pitfalls of its abuse, are reviewed. Reports of epidemics of MS are examined and discarded because they are based on the biologically meaningless date of diagnosis or that of onset, rather than when MS was probably acquired, that is, before puberty. The concept of onset-adjusted prevalence suggests that patients who are symptomatic should be included retrospectively in epidemiological surveys, even before they have been formally diagnosed as having MS, but individuals who were symptomatic before moving to a study area should not. The importance of ethnic homogeneity of patients and control subjects cannot be overemphasized in prevalence and risk factor studies. In the latter, close attention must be paid to biological plausibility and to prudent statistical interpretation. The hypothesis of the MS trait describes a systemic, asymptomatic condition that does not affect the nervous system, and may explain the low concordance of the disease in monozygotic twins.

Brain↗
PubMed1994

The dissemination of multiple sclerosis: a Viking saga? A historical essay.

The highest prevalence rates for multiple sclerosis are found in Iceland, Scandinavia, the British Isles, and the countries settled by their inhabitants and their descendants, that is, the United States, Canada, Australia, and New Zealand. This suggests that the Vikings may have been instrumental in disseminating the genetic susceptibility to the disease in those areas as well as in other parts of the world. The Vikings raided in most European countries and settled in Normandy and in Sicily and southern Italy. They engaged in trade with the Arabs along the river routes to the Caucasus and to the Black and Caspian Seas and penetrated into Persia, India, and probably China. They also migrated to the East and established the Russian state. Under the name Varangians, they became part of the Byzantine army and were active in all of the military activities of the Byzantine Empire. They participated in the Crusades. Russians, many of Scandinavian origin, also constituted a regiment of the Mongol army and roamed throughout that empire as well. The custom of capturing and keeping or selling women and children, which was widespread in the early Middle Ages, as well as the flourishing slave trade in men, were important factors in this genetic dissemination.

Asia↗
PubMed1994

The role of trauma in the pathogenesis of multiple sclerosis: a review.

The suggestion that an alteration of the blood-brain barrier (BBB) is an obligatory step in the pathogenesis of the multiple sclerosis (MS) lesion has been amply confirmed by innumerable magnetic resonance scans. There also exists a large body of clinical, neuropathologic, neuropsychologic, radiologic and experimental evidence that shows that trauma, in particular mild concussive injury to the head, neck or upper back, thus impinging on the brain and spinal cord, may result in an increase in BBB permeability. It is only logical therefore to infer that when such mild trauma to those parts of the body affects MS patients, the resulting alteration of the BBB leads to the formation of new lesions or the enlargement and activation of old ones. In such situations trauma acts as a facilitator of the postulated but still not fully understood pathogenetic mechanism of lesion formation. Because of the extremely poor correlation between site and size of the lesions and clinical manifestations of MS, one cannot expect that every episode of trauma will result in the appearance of new symptoms in an hitherto asymptomatic individual, or the recurrence of old symptoms in an MS patient. It is inappropriate to attempt to prove or disprove a causal relationship between physical trauma and MS exacerbations or clinical onset by means of epidemiologic studies. The unpredictability and variability of the clinical manifestations of the disease, the differences in the genetic and immunologic backgrounds of individuals, as well as in their degree of clinical and pathologic involvement and level of activity, render such investigations pointless.

Accidents, Traffic↗
PubMed1994

Notes on the pathogenesis of multiple sclerosis.

A multifactorial genetic susceptibility determines the risk of acquiring multiple sclerosis (MS). This risk is modified by environmental factors. A viral antigenic challenge, either infectious or vaccinal, causes a genetically susceptible person to develop the MS trait, a systemic asymptomatic condition which does not affect the nervous system. It consists of an activated immune system and increased vulnerability of the blood-brain barrier (BBB). MS may never progress beyond this stage. A second antigenic challenge results in an immune response by means of the phenomenon of molecular mimicry and leads to an alteration of the BBB, an obligatory step in the pathogenesis of the disease. Other occurrences such as trauma or electrical injury, termed facilitators, may also cause this change in the BBB. The exact mechanism for the BBB alteration is unknown, but it allows the penetration into the brain parenchyma of cellular and non-cellular elements of the blood and the formation of the initial MS lesion, i.e., inflammation and edema of the myelin sheath. This stage is fully reversible, but may also proceed to plaque formation by a mechanism which is not yet understood. Myelinoclasia releases myelin components that get into the blood via the altered BBB and elicit an immune response from activated lymphocytes, which may then be involved in further attacks on the myelin sheath and lead to a self-perpetuating progressive illness.

Blood-Brain Barrier↗
PubMed1993

The pathogenesis of multiple sclerosis. Additional considerations.

Multiple sclerosis (MS) is acquired as a systemic "trait" by individuals who are genetically susceptible. This condition does not involve the central nervous system (CNS) and is characterized by a state of hyperactive immunocompetent responsiveness. It develops as the result of an antigenic challenge by a viral protein, either from a viral infection or a vaccination. In order for MS to become a disease affecting the CNS, it is necessary for the blood-brain barrier's (BBB) impermeability to be altered. This is now a fully recognized fact. As a result of this change, the MS lesion, which consists of edema and inflammation occurs. It may but need not lead to demyelination. Several mechanisms can cause this increased permeability of the BBB. The role of the immune system, and in particular of T lymphocytes in initiating and continuing the process of lesion formation remains extremely controversial. In fact, there are unanswered questions regarding the actual target of MS: is it the myelin sheath itself or its forming cell, the oligodendrocyte, or is it the BBB itself leading to bystander demyelination? The role of mild, concussional trauma to the CNS in producing the alteration of the BBB and therefore acting as a trigger or facilitator in the development or enlargement of MS lesions in the CNS, is based on considerable clinical, neuropathological and experimental evidence. Along with another viral infection, it must be one of the commonest causes of progression of MS, and quite often leads to the onset of the clinical manifestations of an hitherto asymptomatic condition.

Amino Acid Sequence↗
PubMed1993

[Multiple sclerosis in the black population].

Numerous epidemiological studies showed that The occurrence of multiple sclerosis (MS) was the result of genetic factors varying by ethnic group as well as geographical and environmental factors. It is difficult to estimate exactly the prevalence of MS among black Africans. Nevertheless it's possible to state that the disease is rare but present among those populations. Among black Americans prevalence of MS seems related to the degree of mixture with white population. Among West Indians the occurrence of MS is closely related to an environmental factor acquired in Europe before 15 years of age. Those data confirm the existence during childhood and adolescence of a critical period during which an environmental factor is acquired in regions of high prevalence for MS.

Adolescent↗
PubMed1992

Improvement in motor evoked potentials and clinical course post-steroid therapy in multiple sclerosis.

Motor evoked potentials (MEP) were recorded in 23 patients with definite relapsing multiple sclerosis before and after treatment with a short course of high dose of methylprednisolone. MEP were performed together with clinical examination just before treatment, and 6 and 60 days later. The following results were observed: (1) a statistically significant relationship between the corticospinal deficit and the alteration in MEP, (2) a significant improvement in latency of MEP by day 6, (3) a significant correlation between the change in the Kurtzke disability scale rating and the improvement in MEP. The results provide further evidence for the possible effectiveness of short courses of high dose corticosteroids in the treatment of relapses of multiple sclerosis and the usefulness of MEP in its assessment.

Adult↗